Congestive heart failure (CHF) is a debilitating disease that is generally initiated by some index cardiac event that results in muscle damage and a decline in cardiac pumping ability. The precipitating index event may be episodic, occurring abruptly, e.g., myocardial infarction; or it may develop gradually over time, e.g., genetic cardiomyopathy. Following the index event, a decline in pumping capacity triggers neurohormonal compensatory mechanisms, which are activated to restore and maintain healthy cardiac output. Due to the effectiveness of these compensatory mechanisms, it is often difficult to recognize the development of persistent underlying disease, as the patient may appear asymptomatic with respect to metrics such as ejection fraction and cardiac output. Nevertheless, evidence of disease may be physically present in the aberrant motion and subsequent remodeling of the failing heart. Left ventricular (LV) remodeling is a progressive phenomenon characterized globally by remodeling of LV chamber size and shape, with a corresponding loss of cardiomyocytes, myocyte hypertrophy and interstitial fibrosis. Left ventricular remodeling dramatically alters the mechanical environment, which in turn influences growth and remodeling processes. It is well established that mechanical stimuli (e.g., stress or strain) are important epigenetic factors in cardiovascular development, adaptation, and disease. Changes in heart structure and function result in changes in the mechanical forces sensed by the cells. This alters the biochemical activity of the cells, which in turn stimulates changes in the structure and function of the heart. Interestingly, abnormal cardiac kinematics is often considered a symptom of heart failure when in actuality it is likely that aberrant motion is a primary contributing factor to the aberrant growth and remodeling i.e., cellular responses to the pathologic mechanical factors lead to further pathologic remodeling and a positive feedback loop emerges such that eventually a threshold is reached wherein the neurohormonal compensatory mechanisms activated to maintain homeostasis are no longer sufficient to deter further progression of the disease. Consequently, treatment strategies that fail to remedy the aberrant mechanical environment become increasingly ineffective as the disease progresses.
There are numerous cardiac devices, artificial hearts, and heart assist devices currently on the market. In addition, other therapies like drugs, biventricular pacing, stem cell therapies, blood contacting assist devices, surgical manipulations, or passive stents and constraints typically off-load the heart and thus only modulate the strain pattern indirectly.
One heart assist device is shown in U.S. Pat. No. 5,119,804, issued on Jun. 9, 1992 to Anstadt, for a cardiac massage apparatus and a drive system. The cardiac massage apparatus includes a cup having a liner that is connected within the cup at its upper and lower ends. Dimensions defining an optimum cup shape as a function of ventricular length are disclosed wherein the heart remains within the cup when mechanically activated.
Other examples include U.S. Pat. Nos. 6,663,558; 6,612,979; 6,612,978; 6,602,184; and 6,595,912, issued to Lau et al., for a cardiac harness to treat congestive heart failure. The harness applies elastic, compressive reinforcement on the left ventricle to reduce deleterious wall tension and to resist shape change of the ventricle during the mechanical cardiac cycle. Rather than imposing a dimension beyond which the heart cannot expand, the harness provides no hard limit over the range of diastolic expansion of the ventricle. Instead, the harness follows the contour of the heart throughout diastole and continuously exerts gentle resistance to stretch.
U.S. Pat. No. 6,602,182, issued on Aug. 5, 2003, to Milbocker, for a unified, non-blood contacting, implantable heart assist system surrounds the natural heart and provides circumferential contraction in synchrony with the heart's natural contractions. The pumping unit includes adjacent tube pairs arranged along a bias with respect to the axis of the heart and bound in a non-distensible sheath forming a heart wrap. The tube pairs are tapered at both ends such that when they are juxtaposed and deflated they approximately follow the surface of the diastolic myocardium. Inflation of the tube pairs causes the wrap to follow the motion of the myocardial surface during systole. A muscle-driven or electromagnetically powered energy converter inflates the tubes using hydraulic fluid pressure. An implanted electronic controller detects electrical activity in the natural heart, synchronizes pumping activity with this signal, and measures and diagnoses system as well as physiological operating parameters for automated operation. A transcutaneous energy transmission and telemetry subsystem allows the Unified System to be controlled and powered externally.
U.S. Pat. No. 6,592,619, issued on Jul. 15, 2003 to Melvin, for an actuation system for assisting the operation of the natural heart. The system includes a framework for interfacing with a natural heart, through the wall of the heart, which includes an internal framework element configured to be positioned within the interior volume of a heart and an external framework element configured to be positioned proximate an exterior surface of the heart. The internal framework is flexibly suspended with respect to the external frame. An actuator system is coupled to the framework and configured to engage an exterior surface of the heart. The actuator system includes an actuator band extending along a portion of a heart wall exterior surface. The actuator band is selectively movable between an actuated state and a relaxed state and is operable, when in the actuated state, to assume a predetermined shape and thereby indent a portion of the heart wall to affect a reduction in the volume of the heart. A drive apparatus is coupled to the actuator band and is operable for selectively moving the actuator band between the relaxed and actuated states to achieve the desired assistance of the natural heart.
U.S. Pat. No. 6,224,540, issued on May 1, 2001, to Lederman et al., relates to a passive girdle for heart ventricle for therapeutic aid to patients having ventricular dilatation. A passive girdle is wrapped around a heart muscle which has dilatation of a ventricle to conform to the size and shape of the heart and to constrain the dilatation during diastole. The girdle is formed of a material and structure that does not expand away from the heart but may, over an extended period of time be decreased in size as dilatation decreases.
The foregoing problems have been recognized for many years and while numerous solutions have been proposed, none of them adequately address all of the problems.